Two immune responses imperil pancreatic islet allografts transplanted into subjects afflicted with autoimmune diabetes: 1) the well-described allograft response that is mounted against tissues bearing foreign transplantation antigens and 2) a recurrence of the β-cell-specific autoimmune process responsible for the primary disease. To define the role of autoimmune response to transplanted islets, the possibility of a rejection response must be prevented. To accomplish this in spontaneously diabetic BB rats, we induced neonatal tolerance. We found that recurrent autoimmunity in tolerant BB rats can be prevented by treatment of recipients with the monoclonal antibody OX8 (specific for cytotoxic T-lymphocytes) but not W3/25 (specific for helper T-lymphocytes). These findings provide direct evidence for the role of OX8-bearing lymphocytes in autoimmune diabetogenesis.
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Modulation of Islet Immunogenicity|
January 01 1989
Prevention of Recurrent Diabetes in BB Rats After Islet Transplantation by Monoclonal Antibody Therapy Free
James F Markmann;
James F Markmann
Hospital of the University of Pennsylvania
Philadelphia, Pennsylvania
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Jill D Jacobson;
Jill D Jacobson
Hospital of the University of Pennsylvania
Philadelphia, Pennsylvania
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Kenneth L Brayman;
Kenneth L Brayman
Hospital of the University of Pennsylvania
Philadelphia, Pennsylvania
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Hiromitsu Kimura;
Hiromitsu Kimura
Hospital of the University of Pennsylvania
Philadelphia, Pennsylvania
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Clyde F Barker;
Clyde F Barker
Hospital of the University of Pennsylvania
Philadelphia, Pennsylvania
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Ali Naji
Ali Naji
Hospital of the University of Pennsylvania
Philadelphia, Pennsylvania
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Address correspondence and reprint requests to James F. Markmann, c/o Dr. Ali Naji, Hospital of the University of Pennsylvania, 3400 Spruce Street, Philadelphia, PA 19104
Citation
James F Markmann, Jill D Jacobson, Kenneth L Brayman, Hiromitsu Kimura, Clyde F Barker, Ali Naji; Prevention of Recurrent Diabetes in BB Rats After Islet Transplantation by Monoclonal Antibody Therapy. Diabetes 1 January 1989; 38 (Supplement_1): 165–167. https://doi.org/10.2337/diab.38.1.S165
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